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Tan, Joel M. J.; Garner, Monica E.; Regeimbal, James M.; Greene, Catherine J.; Márquez, Jorge D. Rojas; Ammendolia, Dustin A.; McCluggage, Adam R. R.; Li, Taoyingnan; Wu, Katherine J.; Cemma, Marija; Ostrowski, Philip P.; Raught, Brian; Diamond, Michael S.; Grinstein, Sergio; Yates, Robin M.; Higgins, Darren E.; Brumell, John H.

Listeria exploits IFITM3 to suppress antibacterial activity in phagocytes

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  • Media type: E-Article
  • Title: Listeria exploits IFITM3 to suppress antibacterial activity in phagocytes
  • Contributor: Tan, Joel M. J.; Garner, Monica E.; Regeimbal, James M.; Greene, Catherine J.; Márquez, Jorge D. Rojas; Ammendolia, Dustin A.; McCluggage, Adam R. R.; Li, Taoyingnan; Wu, Katherine J.; Cemma, Marija; Ostrowski, Philip P.; Raught, Brian; Diamond, Michael S.; Grinstein, Sergio; Yates, Robin M.; Higgins, Darren E.; Brumell, John H.
  • imprint: Springer Science and Business Media LLC, 2021
  • Published in: Nature Communications
  • Language: English
  • DOI: 10.1038/s41467-021-24982-0
  • ISSN: 2041-1723
  • Keywords: General Physics and Astronomy ; General Biochemistry, Genetics and Molecular Biology ; General Chemistry ; Multidisciplinary
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:p>The type I interferon (IFN) signaling pathway has important functions in resistance to viral infection, with the downstream induction of interferon stimulated genes (ISG) protecting the host from virus entry, replication and spread. <jats:italic>Listeria monocytogenes</jats:italic> (<jats:italic>Lm</jats:italic>), a facultative intracellular foodborne pathogen, can exploit the type I IFN response as part of their pathogenic strategy, but the molecular mechanisms involved remain unclear. Here we show that type I IFN suppresses the antibacterial activity of phagocytes to promote systemic <jats:italic>Lm</jats:italic> infection. Mechanistically, type I IFN suppresses phagosome maturation and proteolysis of <jats:italic>Lm</jats:italic> virulence factors ActA and LLO, thereby promoting phagosome escape and cell-to-cell spread; the antiviral protein, IFN-induced transmembrane protein 3 (IFITM3), is required for this type I IFN-mediated alteration. <jats:italic>Ifitm3</jats:italic><jats:sup>−/−</jats:sup> mice are resistant to systemic infection by <jats:italic>Lm</jats:italic>, displaying decreased bacterial spread in tissues, and increased immune cell recruitment and pro-inflammatory cytokine signaling. Together, our findings show how an antiviral mechanism in phagocytes can be exploited by bacterial pathogens, and implicate IFITM3 as a potential antimicrobial therapeutic target.</jats:p>
  • Access State: Open Access